title: Something more to say about calcium homeostasis: the role of vitamin K2 in vascular calcification and osteoporosis.
abstract: BACKGROUND
  Vascular calcification and osteoporosis share similar etiopathogenetic mechanisms. Vitamin K2 deficiency could be responsible of the so called "calcium paradox", that is the lack of calcium in the bone and its storage in the vessel wall. These events may have clinically relevant consequences, such as cardiovascular accidents, and bone fractures.
  
  
  OBJECTIVE
  To review the biological function of vitamin K2 metabolism, the main factors related to its deficiency and the consequent clinical significance.
  
  
  CONCLUSIONS
  Vitamin K2 is essential for the function of several proteins, involved in the maintenance of the normal structure of arterial wall, osteoarticular system, teeth, and for the regulation of cell growth. It has been demonstrated to have a pivotal role in the inhibition of vascular foci of calcification, and in the regulation of calcium deposition in the bone. Vitamin K2 deficiency is often subclinic in a large part of healthy population. This deficiency is related to the interaction of various factors, such as the reduced dietary intake, the alteration of intestinal absorption or production, with a possible role of intestinal microbiota and the increased consumption at the vessel wall.
  
  
  CONCLUSIONS
  Vitamin K2 deficiency has recently been recognized as a protagonist in the development of vascular calcification and osteoporosis. Data reported so far are promising and, dietary supplementation seems a useful tool to contrast these diseases. However, large studies or solid clinical correlations regarding vitamin K2 deficiency and its pathologic consequences are needed to confirm these preliminary experiences.
authors.affiliation: Internal Medicine and Angiology, Catholic University of Sacred Heart, A. Gemelli Hospital, Rome, Italy. francesca.ponziani@yahoo.it.
authors.forename: R
authors.initials: R
authors.lastname: Flore
authors.forename: F R
authors.initials: FR
authors.lastname: Ponziani
authors.forename: T A
authors.initials: TA
authors.lastname: Di Rienzo
authors.forename: M A
authors.initials: MA
authors.lastname: Zocco
authors.forename: A
authors.initials: A
authors.lastname: Flex
authors.forename: L
authors.initials: L
authors.lastname: Gerardino
authors.forename: A
authors.initials: A
authors.lastname: Lupascu
authors.forename: L
authors.initials: L
authors.lastname: Santoro
authors.forename: A
authors.initials: A
authors.lastname: Santoliquido
authors.forename: E
authors.initials: E
authors.lastname: Di Stasio
authors.forename: E
authors.initials: E
authors.lastname: Chierici
authors.forename: A
authors.initials: A
authors.lastname: Lanti
authors.forename: P
authors.initials: P
authors.lastname: Tondi
authors.forename: A
authors.initials: A
authors.lastname: Gasbarrini
mesh_terms: D002118:Calcium / Q000378:metabolism*; D019587:Dietary Supplements; D006706:Homeostasis; D006801:Humans; D007422:Intestines / Q000382:microbiology; D010024:Osteoporosis / Q000209:etiology*; D061205:Vascular Calcification / Q000209:etiology*; D024482:Vitamin K 2 / Q000378:metabolism*
chemical_list: D024482:Vitamin K 2; D002118:Calcium